Very little is known about how X-linked immune deficiencies (xid) affect various lymphoid cell populations and their functional interactions. The limited heterogeneity of antibodies observed in the immune response of mice to phosphocholine (PC) makes this an excellent model system for observing xid gene induced changes in idiotypic expression. In preliminary studies we have demonstrated that the presence of an xid gene in CBA/N mice or hemizygous F1 male mice results in a loss or low frequency of expression of T15 idiotype positive anti-PC antibodies in these mice. In this research proposal, we outline a series of studies which will help define the affect of the xid gene in CBA/N mice on the immune network which governs the response to phosphocholine. The PC-specific antibodies formed in immune defective and control mice will be analyzed by radioimmunoassay and/or isoelectric focusing for idiotype, isotype, light chain composition, and relative binding site affinity. In addition, the PC-specific B cell repertoire and the frequency of PC-specific B cell precursors will be analyzed using both the splenic focus assay and hybridoma technology. These studies will allow us to compare the serologically expressed B cell repertoire, the functional precursor repertoire, and the cell fusion repertoire of CBA/N and immunologically normal mice. This experimental model also provides a powerful tool for studying the cell type(s) which control the predominant expression of the T15 idiotype in normal mice. Unirradiated, immune defective F1 male mice will accept transfers of normal lymphoid cells from their female littermates; thus, the influence of transfer of purified T and B lymphocytes on the PC idiotype response in immune defective mice will also be characterized.